heart failure management in 2019tnacc.org/wp-content/uploads/2017/04/heart-failure... ·...

Heart Failure Management in 2019

Mark F Aaron, MD, FACC

Disclosures

Speakers Bureau: Novartis

Research: Abbott

None of my discussion will be off label.

A 54-year-old post menopausal woman presents to her PCP for a routine generalmedical exam. She denies any lifestyle restrictions. Her provider heard a systolic murmur. The cardiac exam was otherwise normal. Her primary care provider requests an echocardiogram which demonstrates an LVEF of 32% with global hypokinesis, moderate LV enlargement, and trivial aortic stenosis but no other significant valve disease. Which of the following is the most appropriate medicaltherapy?

a) Beta blocker and sacubitril / valsartan

b) ACE inhibitor and statin

c) ACE inhibitor and beta blocker

d) ACE inhibitor

e) ACE inhibitor, beta blocker, and aldosterone antagonist

A 48-year-old African-American man with known HFrEF (LVEF = 28%) presents with exertional dyspnea climbing a flight of stairs and mild orthopnea. His medical therapy includes metoprolol tartrate 50 mg twice daily, lisinopril20 mg daily, and Lasix 40 mg daily. BP is 122/76 and HR is 76. He is euvolemic on exam. Creatinine is 1.0 and potassium is 4.4.

Which of the following is the most appropriate change to his medical therapy?

a) Start sacubitril / valsartan

b) Start hydralazine and nitrates

c) Stop metoprolol tartrate and transition to carvedilol

d) Start spironolactone

e) Increase furosemide

• 56 year old man with history of MI presents withprogressively increasing dyspnea and lower extremity edema

• ICD-CRT was implanted two years prior to this admission

• His outpatient regimen consists of Lisinopril 5 mg twice daily, carvedilol 3.125 mg twice daily, simvastatin 20 mg daily, aspirin 81 mg daily, spironolactone 25 mg daily and furosemide 80 mg daily

56-Year-Old Male

• On examination he is afebrile, heart rate is 62/min, blood pressure 86/60 mm Hg, JVP is significantly elevated with prominent v waves, lungs are clear, 3/6 pansystolic murmur over the precordium, S3 is present, 3+ pitting edema and cool extremities

• Laboratory tests reveal a hemoglobin of 8 g/dl, sodium 126 mmol/L, potassium 4.5 mmol/L, BUN 42 mg/dl and creatinine 1.9 mg/dl

• Electrocardiogram shows a 100% A-V paced rhythm

• He was admitted to the hospital for further management

56 year old manAll the statements are true regarding this patient’s

management except

1. Decrease carvedilol until hemodynamically stable

2. Right heart catheterization may be indicated

3. Adding metolazone 5 mg orally daily may improve

symptoms

4. Starting IV low dose dopamine may improve renal

blood flow

5. IV furosemide as a continuous infusion is superior in diuretic efficacy to 12 hourly bolus dosing

Objectives

• Describe the evaluation of patients presenting withstable heart failure in the present.

• Use recent guideline directed medical therapy in patients with stable heart failure with reduced EF

• Develop appropriate management strategies for thepatient with stable heart failure with preserved EF

• Recognize the patient with ADHF

• Use recent guidelines to select appropriate medical therapies for patients with ADHF

Framingham Criteria for Clinical Diagnosis of Congestive Heart Failure

• PND

• Orthopnea

• Elevated JVP

• Rales

• S3

• CXR cardiomegaly

• CXR pulm edema

• Major Criteria • Minor Criteria

• Peripheral edema

• Night cough

• DOE

• Hepatomegaly

• Pleural effusion

• HR >120/min

• Wgt loss 4.5 kg in5 days with diuretic

Validated CHF if 2 major or 1 major and

2 minor are present concurrently

ACC/AHA Stages of Heart Failure

At Risk Asymptomatic Symptomatic Heart Failure

Refractory

HF

Structural

heart

disease with

current or

prior signs

or

symptoms of

HF

Structural

heart

disease but

without signs

or symptoms

of HF

At high risk

for HF but

without

structural

heart

disease

Yancy et al: J Am Coll Cardiol, 2013

Stage A Stage B Stage C Stage D

ACCF/AHA Stages of HF and NYHA Functional ClassificationACCF/AHA stages of HF NYHA functional classification

A At high risk for HF but without structural heart disease or symptoms of HF

None

B Structural heart disease but without signs or symptoms of HF

I No limitation of physical activity

C Structural heart disease with prioror current symptoms of HF

No limitation of physical activityII Slight limitation of physical activity III Marked limitation of physical activity IV Unable to carry on physical activity

without symptoms of HF, or symptomsof HF at rest

D Refractory HF requiring specialized interventions

IV Unable to carry on physical activity without symptoms of HF, or symptoms of HF at rest

I

Goals of the Initial Evaluation

Less Common Causes• Amyloid

• SLE, scleroderma

• HCM

• Myocarditis

• Pericarditis

• Thyroid disease

• Diabetes

• Pheochromocytoma

• Postpartum

• Hemochromatosis

• Sarcoid

Etiology

Common Causes• Coronary artery disease

• Hypertension

• Valvular heart disease

• Tachycardia mediated

• Chemotherapy / radiation

• Alcohol / other toxins

History

• Potential clues regarding the etiology

• Alcohol, illicit drug use

• Chemotherapy / radiation

• Angina

• Palpitations (tachycardia induced CM); syncope

• Family history*

• Functional Status

• Volume status and hemodynamics

• Orthopnea, ascites, early satiety, bendopnea

* Two or more 1st degree familymembers

Physical Exam

• General: SOB, cachexia, Δ MS, cyanosis

• VS: tachycardia, BP (orthostatics)

• JVP: volume status / filling pressures,AJR

• Lungs: usually clear ± effusions

• Heart: soft S1, loud P2, MR/TR murmurs (±), gallops, palpation for apical and RV impulses

• Abdomen: pulsatile hepatomegaly, ascites

• Ext: edema, cold (high SVR), pallor

• Vascular: pulsus alternans (low output)

Diagnostic Evaluation

• Laboratory (class I)

• Renal function, lytes, CBC, LFTs, TSH, UA, HbA1c, lipids, NT-proBNP*

• Chest radiography (class I)

• Cardiomegaly, pulmonary edema

• Electrocardiogram (class I)

• Rhythm, QRS duration

• Overnight oximetry (class IIa)

• CPAP if OSA; avoid ASV in central sleep apnea

* Can be normal in HFpEF

Transthoracic Echocardiogram

*HFpEF: LVH, LA dilatation, diastolic dysfunction

Transthoracic Echocardiogram

Three questions:

1. What is the EF (reduced or preserved)?

• HFrEF < 40%

• HFpEF* > 50%

2. LV size and structure normal or abnormal?

3. Any other structural abnormalities (RV, valves,pericardium)?

Repeat Assessment of EF

• Obtain repeat EF after a major change in clinical status orafter optimizing medical Rx, typically 3-6 months (class IIA)

• Implications for device therapy

• Routine repeat measurement of LV function assessment in the absence of clinical status change ortreatment interventions should not be performed (class III)

Assessment for CAD

• Coronary angiography

• Class I if angina or known ischemia

• Class IIa if atypical CP, known,or suspected CAD

• Noninvasive stress imaging

• Class IIa if known CAD but no angina

• Class IIb to define likelihood of CAD

• Wall motion/perfusion defects common in non ischemic HF

Other Evaluation

• Other labs (class IIa), especially for those at risk:

• Iron studies, HIV, protein electrophoresis, autoimmune serologies and inflammatory markers, endocrine/metabolic

• Cardiac MRI – may be useful in iron overload, sarcoid,myocarditis, viability, pericardial disease

• PET – if concern for sarcoid (active disease)

• Cardiopulmonary exercise testing

• Determine cardiac versus non-cardiac cause of symptoms and quantify severity in consideration of advanced therapies (<14 mL O2/kg*min)

Endomyocardial Biopsy

• Usually not indicated in systolic HF –(class III for routine evaluation of systolic HF)

• Only useful if results are likely to influence therapy

• Sarcoidosis

• Infiltrative cardiomyopathies

• Amyloidosis

• Hemochromatosis

• Giant cell myocarditis

Goal of Therapies in HF with Reduced EF

CHFNormal

Reverse remodeling

Left ventricular volume

Left

ventr

icula

r pre

ssure

ACC/AHA Stages of Heart Failure

At Risk Asymptomatic Symptomatic Heart Failure

DT-VAD,

Transplant,

Palliation

Address Risk Factors*

-Hypertension

-CAD

-Diabetes

http://www.hfsa.org/wp-content/uploads/2015/04/HFSA-2010-HF-Guidelines-Section-03.pdf


HFSA 2010 Guidelines

Stage A Stage B Stage C Stage D

http://www.hfsa.org/wp-content/uploads/2015/04/HFSA-2010-HF-Guidelines-Section-03.pdf

Wang et al: Circulation, 2003

Stage B

1.0

0.8

0.6

0.4

0.2

0.00 2 4 8 10 126

Years

Surv

ival

No ALVD (EF >50%) and no HF history

Mild ALVD (EF 40% to 50%)

Moderate to severe ALVD (EF <40%)

Systolic HF (EF 50%)

Stage B

ACEi orARB

(class I)

Beta blocker

(class I)

Yancy et al. J Am Coll Cardiol, 2013

Stage B

ACEi orARB

(class I)

• Improved mortality and morbidity*

• Start with ACEi

• ARB✝ when ACEicontraindicated

• Routine combination ACEi /ARB contraindicated (class III)

*SOLVD-Prevention http://www.ncbi.nlm.nih.gov/pubmed/12788569✝studied in Stage B HFrEF with prior MI; no data in absence ofMI


http://www.ncbi.nlm.nih.gov/pubmed/12788569


Stage B

Beta Blocker

(class I)

• Improved mortality*

• No class effect

• Preferred agents:

• Carvedilol

• Metoprolol succinate

• Bisoprolol

*CAPRICORN http://www.ncbi.nlm.nih.gov/pubmed/11356434

http://www.ncbi.nlm.nih.gov/pubmed/11356434

Carvedilol vs Metoprolol SuccinateCarvedilol Metoprolol succinate

Dosing Low-dose responsiveness

Goal dose = 25 mg BID

Once daily dosing

Goal dose = 200 mg QD

Blood pressure effect • Greater BP ↓ actions

• Use in setting of concomitant

hypertension

• Preferred agent when BP not

limitation

• Less BP ↓ actions

• May facilitate up-titration

of other meds

Specific populations • Less insulin resistance Less bronchospasm

Bisoprolol similar to metoprolol succinate.

ACEi orARB

(class I)

Stage C

Aldosterone

Antagonists

(class I)

Beta Blocker

(class I)

ARNI

(class I)

Hydralazine

/ NitratesDigoxin

Diuretic(s)

Special Populations:

If Volume Overloaded:

Ivabradine

Yancy et al: J Am Coll Cardiol, 2013 and 2017

Aldosterone Antagonists

• NYHA Class II-IV with EF < 40% (class I)

• Follow potassium closely; do not initiate if > 5; recheck after 3 days, weekly for 1 month, then monthly for three months (HFSA guidelines)

• Avoid if Cr >2.5 in men and >2 in women (ACC guidelines)

• Start with spironolactone

• Transition to eplererone if gynecomastia with spironolactone


HFSA 2010 Guidelines

Loop Diuretics

Agent

Initial daily

dose (mg)

Max total daily

dose (mg) Bioavailability (%)

Duration of

action (hr)

Furosemide20-40 qd or

bid600 10-100% 4-6

Bumetanide0.5-1.0 qd or

bid10 80-100% 6-8

Torsemide 10-20 qd 200 80-100% 12-16

Ethacrynic acid25-50 qd or

bid200 90-100% 6

Consider torsemide or bumetanide in right-sided HF due to more consistent bioavailability.

Ethacrynic acid with sulfa allergy; very expensive (particularly intravenous).

Brater, NEJM, 1998

Thiazide Diuretics

• Use in conjunction with loop diuretics

• SEVERE electrolyte disturbances

• Hypokalemia

• Consider supplement / K sparing diuretic

• Hypomagnesemia

• Hyponatremia

• Azotemia

• Careful with daily dosing

Intensifying Diuresis as an Outpatient

• Ensure adherence, assess for precipitants

• Double daily loop diuretic dose

• Triple daily loop diuretic dose

• Twice daily loop diuretic dosing

• Transition to an alternative loop diuretic (torsemide or bumetanide)

• Add a thiazide

• Outpatient IV diuresis

Inte

ns

ity

Hydralazine / Nitrates

• Class I for persistently symptomaticAfrican-Americans(despite ACEi and beta blocker therapy)

• Class IIa for patients intolerant or ACEior ARB due to renal dysfunction or hyperkalemia


The Digitalis Investigation Group. NEJM. 1997

Digoxin

• Consider if LVEF <40%; decrease HF-related hospitalizations (class IIa)

• Consider in AF with suboptimalheart rate control despite(or intolerant to) beta blocker

• Goal level 0.5 to 0.9 ng/ml2

Yancy et al. J Am Coll Cardiol, 2013HFSA 2010 Guidelines

D. Purrpuria

2016 (and 2017) ACC / AHA HF Guideline Update

• Sacubitril / valsartan (ARNI)

• Ivabradine


NT-proBNP

(biologically

inactive)

Pro-BNP

BNP

(biologically

active)

Neurohormonal activation

Vasodilatation

Cardiac fibrosis, hypertrophy

Natriuretic

Inactive metabolites

Neprilysin* sacubitril inhibits

neprilysin

• Neprilysin also mediates degradation of bradykinin, substance P, adrenomedullin, calcitonin gene related peptide

Sacubitril Mechanism of Action

Sacubitril / Valsartan

• Paradigm-HF published in 2014, FDA approved in 2015

• ACC / AHA focused HF guideline update in 2016 and 2017

• Class I indication for patients with chronic symptomatic HFrEF (NYHA class II or III)

• 20% RRR in HFH and CV Death beyond Enalapril

• Avoid if history of angioedema

• Hold ACE or ARB for 48 hours prior to starting


HFrEF Mortality With Medical Therapy


Pitt et al: NEJM, 1999 Fonarow et al: JAMA Cardio. 2016

0

-10

-20

-30

-40

-50

-60

-70

-80

-90

-100

ACE

inhibitors+ Beta

blockers+ Aldo

blockers + ARNi

Cum

ula

tive %

decre

ase

Additional34%

BeyondACEi

NNT=9

Additional

30% *

NNT=6

17%

NNT = 26

Additional

16%

Beyond GDMT

NNT=27

NNT for mortality standardized to 36 months

* Beta blocker use 10-11%

Ivabradine

• Inhibits the If current in the sinoatrial node, reduces heart rate

• SHIFT trial (published 2010): reduced HF admissions among EF< 35%, NYHA II-IV, sinus rhythm, HR > 70; no mortality benefit

• FDA approved in 2015

• IIa recommendations in the 2016 ACC / AHA HF guideline update

• Ensure goal beta blocker dose before starting

Yancy et al. J Am Coll Cardiol, 2016. Swedberg et al. Lancet. 2010.

Tips to Optimize Medical Therapy

• Go slow (marathon, not a sprint); increase insmall increments every 1-2 weeks

• Tolerate asymptomatic hypotension

• Diuretic requirements may decrease with positive remodeling

• “Treat the patient, not the creatinine”

• Share the Seattle Heart Failure Model with the patient topromote buy-in with medical therapy

• Repeat TTE 3-6 months after med optimization

Drugs to Avoid in HFrEF

• NSAIDs

• Calcium channel blockers (except amlodipine)

• Most antiarrhythmics (except amiodarone and dofetilide)

• Thiazolidinedione

Lifestyle and Non-Medical Interventions

• Sodium restriction: < 2 grams per day

• Fluid restriction: < 2 liters per day

• Exercise: 30 minutes, 5 times per week

• EtOH: ideally abstinence, otherwise ≤ 2 week

• Goals of care discussion and end of life

discussion: never too early

Guidelines for Treatment of HFpEF…

2005 similar to 2001



HFpEF not addressed in 2016

Slide Adapted from Margaret Redfield

HFpEF Medical Therapy

• Class I

• Control hypertension

• Diuretics if volume overload

• Class IIa

• ACEi, ARB, and Beta blockers as first line hypertension therapy

• Manage AF according to guidelines

• Revascularize if angina or significant ischemia

• Class IIb – ARBs may reduce hospitalization


Negative Trials in HFpEF

• RELAX –sildenafil

• NEAT HF –Isosorbide mononitrate

• CHARM,I-PRESERVE –ACE / ARBs

• TOPCAT –spironolactone*

0.00

0.20

0.40

0.60

0 2 4 6

Years

Death

or

HF

adm

issio

n

Placebo

Spironolactone

Americas

Russia/Georgia

Pfeffer et al: Circulation, 2014

Clinical Pearls for Treatment of HFpEF

• Focus on aggressive treatment of hypertension(ACE or ARB preferred)

• Diuretics for volume overload

• If atrial fibrillation present and persistent symptoms, then trial of rhythm control

• Exercise program

• Aldosterone antagonist likely is beneficial

ADHF is….

• Frequent

• Leading medical Medicare discharge Dx, avg LOS 5 days

• Fatal

• ADHERE/EuroHeart 4-7% hospitalized mortality

• 30 day mortality 8-14%, 1 yr 26-37%

• Formidable

• Readmission rates: 20-25% 60 day, ~50% 6 month

JACC 46:1, 57, Eur J HF 2(2):123,JAMA 287:1531.

Progression of Heart Failure

Time

Functionals

tatu

s

Death

Excellent

Heart failure care

1 45

Sudden death event

2

Transplant or ventricular assist device

Supportive care

3

Goodlin et al: J Cardiac Failure 10:200, 2004

Whom to hospitalize?

• Hemodynamically unstable

• Tachycardia, i.e., >120 bpm

• Symptomatic hypotension, SBP<80 mm

• Tachypnea/hypoxia

• Cardiogenic shock

• Altered mentation

• Failed outpatient Rx

• No improvement in dyspnea, edema or weight gain

• Worsening CKD without improvement in symptoms

Causes of Decompensation in HF

%

Noncompliance 42

Ischemia 13

Inadequate pre-treatment 12

Arrhythmia 6

Miscellaneous 6

Hypertension 6

No definite factor 15

Other Causes of Decompensation in HF

• Addition of negative inotrope

• Thyroid abnormalities

• Infection (particularly viral)

• Anemia

• Iatrogenic volume overload

• Cardiotoxins: alcohol, cocaine, certain chemotherapy

• Right ventricular pacing induced dyssynchrony.

But remember…..

• Pulmonary rales may be absent

• Edema may be absent

• BNP levels may not always be elevated

• PND and orthopnea are reliable symptoms

• Weight gain

• JVP is a reliable sign

Recognize In-Hospital Mortality in ADHF

J Am Coll Cardiol. 2005 Jul 5;46(1):57-64, Circ Heart Fail. 2016 Aug;9(8).

• ADHERE: BUN > 43 mg/dl, SBP < 115 mmHg, Scr > 2.75

• Mortality ↑ from 2.1 → 21.9%

• OPTIMIZE-HF: SBP<100 mmHg + Scr > 2 = 16.3% mortality

• GWTG-HF Risk Score

• Score <33 <1% probability of death, score >79 >50%

Advanced Rx

Palliative and Hospice Evaluation

Yes

Congestion?

No

DryandWarm

WetandWarm

DryandCold

WetandCold

Adequateperfusion?Pulse pressure,

cool extremities,altered mentation

Orthopnea, rales, JVD, ascites, edema, weights, I/O

No Yes

Nohria A: Am J Cardiol 2005 [suppl]

No Yes

Yes

Adequateperfusion?

No

DryandWarm

Wet

Warm

DryandCold

WetandCold


Diurese

+vasodilate, tap

Adequateperfusion?

Congestion?

No Yes

Yes

Conge

stion?Adequateperfusion?

No

DryandWarm

WetandWarm

DryandCold


Diurese, Inotropes, Vasodilate

No Yes

Yes

Adequateperfusion?

No

DryandWarm

WetandWarm

WetandCold


Inotropes,

VAD, Txp

No Yes

Yes

Conge

stion?Adequateperfusion?

No

Warm

WetandWarm

DryandCold

WetandCold


Non-Cardiac?

Diuretic Dosage in “Naive”

• Furosemide 20-40 mg IV

• Torsemide 10-20 mg IV

• Bumetanide 1 mg IV

• Double at 2-hour intervals to response or maximal dose

• CKD may require higher bolus (i.e., up to 200 mg Furosemide)

Diuretic Dosage in “Wise”

• Initial IV dose should be equal to or greater than (2.5x)maintenance oral dose

• e.g., 40 mg oral furosemide = IV bolus of 40-100 mg

• Diuretic conversion:

• Torsemide 20 mg = furosemide 40 mg

• Bumetanide 1 mg = furosemide 40 mg

Diuretics

• Guidelines favor beginning diuresis in the ED

• Bolus vs Continuous Infusion?

• DOSE: Continuous infusion equivalent to 12 hourly bolusfurosemide on symptoms and renal function

• Goal urine output should be 3-5 liters per day

Diuretic Resistant?

• Ultrafiltration or HD may be considered in diureticunresponsive pts

• UF: No clear benefit upfront over diuresis

• Does not preserve renal function compared to diuresis

• Consider safety, cost, access, staffing

• UF is reserved for congested patients unresponsive to aggressive diuresis

Inotropic Therapy

• Dobutamine: Primary action beta-1 adrenergic receptors

• ↑SV, ↑CO, modest drop in SVR/LV filling

• Hypersensitivity myocarditis with chronic use

• Milrinone: PDE inhibitor

• Not as impacted by concomitant beta-blockade

• Dopamine: Low dose renal/mesenteric dopamine-1

• Data supporting renal impact/protection limited

JAMA. 2013;310(23):2533.

Use of Inotropes

• Class I in cardiogenic shock

• Class IIa as bridge to transplant

• Class IIb for stage D patients as palliative therapy

• Class IIb indication to improve end organ perfusion in low output patients who have hypotension

• Use of low dose dopamine to improve diuresis is considereda Class IIb indication

ACC/AHA guidelines, 2013

Cardiorenal Syndrome

Declining renal fxn typically with diuretic resistance• Congestive rx limited by decline in GFR

• Measured best by GFR rather than creatinine

• Risks: DM, older age, CKD (GFR<60, ≈ 30-60% of HF)

• Develops in 25-30% of ADHF

• Causes?

• Diuretic induced drop in GFR

• Systemic congestion

• Fall in SBP

Advanced or Refractory Heart Failure

• Fluid status management: requiring renal replacement?

• Not tolerating RAAS or SNS antagonism?

• Referral to HF center

• Transplant, VAD

• Continuous infusion of palliative inotrope?

• Discuss end-of-life care options, advanced directives,goals of treatment

Ross J et al: Circulation Heart Fail, 2010

23% of Medicare beneficiaries readmitted

after a ADHF hospitalization within 30 days

Risk for Recurrence

• In most patients with ADHF, factors leading to admissioncan be identified and potentially mitigated

• Non-compliance higher in the elderly

• Cognitive function, medical literacy

• Comorbidities more frequent in elderly (HTN, CKD, COPD)

• Excess alcohol, non-cardiac medication (NSAIDS, TZDs)

• OPTIMIZE-HF 60% identifiable precipitant

JACC 2008:52:347-56

High Risk for Readmission

• CKD

• Low output state

• DM

• COPD

• Persistent NYHA III/IV

symptoms

• ≥7 Medications

• Substance Abuse

• Frequent admissions

• Multiple active

comorbidities

• Depression/cognitive

impairment

• HD/ESLD/HIV/CVA

• Metastatic CA, active

hematologic CA

• Inadequate social

support, poor health

literacy, or persistent

noncompliance

Diuretic-Based Clinical Strategies Have We Achieved Euvolemia?

7 6

13

24

33

16

3 2

0

10

20

30

40n=51,013

Dis

ch

arg

es

(%)

-20 or more -20 to -15 -15 to -10 -10 to -5 -5 to 0 0 to 5

Change in weight (lbs)

5 to 10 >10

89% reported asymptomatic/improved

Yet 56% had minimal or no weight loss

European Heart Journal Supplements 7:B13–B19

Goals for Dismissal

• Optimize heart failure medications

• Assess readmission risk

• Consider readmission risk tools

• Coordinate transition and dismissal planning

A 54-year-old female presents to her primary care provider for a routine generalmedical exam. She is post menopause. She denies any lifestyle restrictions. Her provider heard a systolic murmur. The cardiac exam was otherwise normal. Her primary care provider requests an echocardiogram which demonstrates an LVEF of 32% with global hypokinesis, moderate LV enlargement, and trivial aortic stenosis but no other significant valve disease. Which of the following is the most appropriate medical therapy?

a) Beta blocker and sacubitril / valsartan

b) ACE inhibitor and statin

c) ACE inhibitor and beta blocker

d) ACE inhibitor

e) ACE inhibitor, beta blocker, and aldosterone antagonist

A 48-year-old African-American man with known HFrEF (LVEF = 28%) presents with exertional dyspnea climbing a flight of stairs and mild orthopnea. His medical therapy includes metoprolol tartrate 50 mg twice daily, lisinopril20 mg daily, and Lasix 40 mg daily. BP is 122/76 and HR is 76. He is euvolemic on exam. Creatinine is 1.0 and potassium is 4.4.

Which of the following is the most appropriate change to his medical therapy?

a) Start sacubitril / valsartan

b) Start hydralazine and nitrates

c) Stop metoprolol tartrate and transition to carvedilol

d) Start spironolactone

e) Increase furosemide

• 56 year old man with history of MI presents withprogressively increasing dyspnea and lower extremity edema

• ICD-CRT was implanted two years prior to this admission

• His outpatient regimen consists of Lisinopril 5 mg twice daily, carvedilol 3.125 mg twice daily, simvastatin 20 mg daily, aspirin 81 mg daily, spironolactone 25 mg daily and furosemide 80 mg daily

56-Year-Old Male

• On examination he is afebrile, heart rate is 62/min, blood pressure 86/60 mm Hg, JVP is significantly elevated with prominent v waves, lungs are clear, 3/6 pansystolic murmur over the precordium, S3 is present, 3+ pitting edema and cool extremities

• Laboratory tests reveal a hemoglobin of 8 g/dl, sodium 126 mmol/L, potassium 4.5 mmol/L, BUN 42 mg/dl and creatinine 1.9 mg/dl

• Electrocardiogram shows a 100% A-V paced rhythm

• He was admitted to the hospital for further management

56 year old manAll the statements are true regarding this patient’s

management except

1. Decrease carvedilol until hemodynamically stable

2. Right heart catheterization may be indicated

3. Adding metolazone 5 mg orally daily may improve

symptoms

4. Starting IV low dose dopamine may improve renal

blood flow

5. IV furosemide as a continuous infusion is superior in diuretic efficacy to 12 hourly bolus dosing

heart failure management in 2019tnacc.org/wp-content/uploads/2017/04/heart-failure... ·...

Documents